Polycystic Kidney Disease (PKD)

• Polycystic Kidney Disease (PKD) is a genetic disorder
• PKD leads to multiple fluid-filled cysts forming in the kidneys
• These cysts enlarge, causing kidney enlargement and nephron destruction
• Kidney failure is the eventual result of this disease

Epidemiology

• 1 in 600,000 people in the US have PKD
• 12.5 million people worldwide have PKD
• PKD represents 10-15% of chronic renal disorders
• There is a 50% genetic inheritance rate
• PKD typically appears between 30-40 years of age
• Men and women are equally affected
• Both kidneys are involved

Pathophysiology

• PKD1 and PKD2 genes encode polycystin-1 (PC1) and polycystin-2 (PC2)
• PC1 and PC2 are proteins involved in renal tubular cell signaling
• These proteins regulate mechanosensation, calcium signaling, and cellular proliferation
• Mutations in PKD1 or PKD2 disrupt normal ciliary function
• Increased cAMP levels stimulate fluid secretion and cyst enlargement
• Dysregulation of calcium homeostasis leads to increased proliferation of tubular epithelial cells
• Loss of planar cell polarity leads to abnormal cell division and cyst growth

Types of PKD

Autosomal Dominant PKD (ADPKD)

• Most common form, affecting 1 in 500-1,000 live births
• Symptoms appear in adulthood, typically between 30-50
• Mutations in PKD1 (85%) or PKD2 (15%) genes
• PKD1 mutations result in a more severe disease course than PKD2 mutations

Autosomal Recessive PKD (ARPKD)

• Less common, affecting 1 in 20,000 live births
• Symptoms appear in infancy or early childhood
• Mutation in the PKHD1 gene, affecting the fibrocystin protein
• ARPKD leads to severe renal dysfunction and congenital hepatic fibrosis

Progression and Pathological Effects

• Cysts originate from renal tubules and progressively enlarge
• Cysts become separated from the nephron leading to fluid accumulation and expansion
• Expanding cysts compress surrounding tissue, leading to ischemia and progressive nephron loss
• This results in interstitial fibrosis and chronic inflammation

Vascular and Systemic Effects

• Renal blood flow is reduced, stimulating the renin-angiotensin-aldosterone system (RAAS)
• RAAS activation results in hypertension, common in 75-80% of PKD patients
• Chronic hypertension accelerates glomerular sclerosis and kidney damage

Extra-Renal Manifestations

• Hepatic cysts are the most common extrarenal feature
• Pancreatic cysts may be seen
• Intracranial aneurysms (risk of subarachnoid hemorrhage)
• Cardiac valve abnormalities (mitral valve prolapse)
• Colonic diverticulosis (risk of rupture)

Clinical Manifestations

• Hypertension
• Hematuria
• Lower back or flank pain
• Headaches
• Abdominal pain
• There may be no signs or symptoms in early stages
• Hypertension r/t damage of renal structures
• Hematuria r/t rupture of cysts
• Progresses to end-stage renal disease (ESRD) 50% of the time

Polycystic Kidney Disease Management

• Medical management focuses on treatment
• Hemodialysis is required if progress to chronic kidney disease (CKD)
• Managing urinary tract infection (UTI) with antibiotics is necessary
• PKD increases the risk of UTIs due to urinary stasis from cystic compression

Antibiotics for UTI's

• Fluoroquinolones are used:
  • Examples: Ciprofloxacin, Levofloxacin
  • MOA: Inhibits bacterial DNA gyrase, prevents DNA replication
  • Indications: Pyelonephritis, recurrent UTIs
  • Contraindications: Renal failure, pregnancy
  • Side Effects: Tendon rupture (Black Box Warning), QT prolongation (arrhythmias)
• Trimethoprim-Sulfamethoxazole (Bactrim) is another choice
  • MOA: Inhibits bacterial folate synthesis
  • Indications: Lower UTI, mild infections
  • Contraindications: G6PD deficiency (risk of hemolysis)
  • Side Effects: Hyperkalemia, rash

Pain Management

• Pain in PKD is caused by cyst expansion, infection, or nephrolithiasis
  • Acetaminophen (Tylenol) is preferred as a first-line treatment for mild to moderate pain
  • NSAIDs (Ibuprofen, Naproxen) should be avoided as they reduce renal perfusion and worsen kidney function

Hypertension Management

• ACE Inhibitors (Lisinopril, Enalapril, Ramipril)
  • Mechanism of Action (MOA): Inhibits angiotensin-converting enzyme (ACE), reducing the production of angiotensin II
  • This leads to vasodilation, reduced sodium retention, and decreased blood pressure
  • Indications: First-line therapy for hypertension in PKD, reduces proteinuria, slowing kidney damage
  • Contraindications: Severe renal impairment (GFR <30 mL/min), Hyperkalemia (risk of potassium retention)
  • Side Effects: Hyperkalemia, Dry cough (due to bradykinin accumulation), Angioedema (rare but life-threatening)

Angiotensin II Receptor Blockers (ARBs) (Losartan, Valsartan, Irbesartan)

• Blocks angiotensin II receptors, preventing vasoconstriction
• Lowers BP and reduces proteinuria
• Indications: Alternative to ACE inhibitors
• Side Effects: Hypotension and Hyperkalemia

Advanced PKD

• When PKD progresses to chronic kidney disease (CKD) stage 5, renal replacement therapy is required
• A Kidney transplant is the definitive treatment for ESRD in PKD and requires lifelong immunosuppression (Tacrolimus, Mycophenolate, Prednisone)
• Dialysis removes waste and excess fluids
  • Hemodialysis uses a dialyzer to remove waste and excess fluids (requires vascular access)
  • Peritoneal Dialysis uses the peritoneal membrane to filter waste via diffusion

Pyelonephritis

• 12 to 13 cases annually per 10,000 in females
• 2 to 3 cases per 10,000 in males
• Women are disproportionately affected r/t sexual activity and UTIs
• Infants and older adults are also more susceptible due to anatomic variations and hormone status

Risk Factors

• Multiple pre-existing UTIs (treated or untreated)
  • Vesicoureteral reflux: Retrograde flow of urine from bladder to the ureters
  • Obstructions: Benign prostatic hypertrophy (BPH), a stricture, or a urinary stone
  • Long-term indwelling urinary catheter
  • Pregnancy is implicated in development of acute pyelonephritis
  • Sexual activity in women

Pathophysiology

• Pyelonephritis is a bacterial infection that affects the renal pelvis, tubules, and interstitium
• It can be acute or chronic, leading to renal scarring, fibrosis, and eventual kidney dysfunction if not properly managed

Types of Pyelonephritis

Acute Pyelonephritis (APN)

Sudden onset and severe infection commonly caused by ascending urinary tract infections (UTIs) - Can lead to sepsis and acute kidney injury (AKI) if untreated

Chronic Pyelonephritis (CPN)

Recurrent or persistent kidney infection that leads to renal scarring, interstitial fibrosis, and nephron loss

• Associated with urinary tract obstructions, vesicoureteral reflux (VUR), or anatomical abnormalities

Pathogenesis of Pyelonephritis

Bacterial Entry and Colonization

• Bacterial Entry and Colonization
  • Most cases are caused by an ascending UTI, where bacteria travel from the urethra → bladder (cystitis) → ureters → kidneys Escherichia coli (80-90%) is usually the culprit - Uropathogenic E. coli (UPEC) contains fimbriae (P pili) that allow it to attach to renal epithelium
    • Proteus mirabilis Produces urease, leading to alkaline urine and struvite stone formation
    • Klebsiella pneumoniae, Enterococcus faecalis and Pseudomonas aeruginosa are pathogens that are more common in hospitalized or catheterized patients

Neutrophilic Infiltration and Inflammation

• Innate immune response activates neutrophils, releasing inflammatory cytokines (IL-6, TNF-α, IL-8) - Leads to renal parenchymal damage and formation of pus (pyuria) in the collecting system

Vasoconstriction and Ischemic Injury

• Endothelial dysfunction due to cytokine release leads to reduced renal blood flow - If untreated, microabscesses form in the renal cortex and medulla

Fibrosis and Chronic Injury

Recurring or untreated pyelonephritis cause tubulointerstitial fibrosis and permanent renal scarring

• This may cause hypertension, chronic kidney disease (CKD), and nephron loss

Clinical Manifestations

Symptoms of Acute Pyelonephritis

• High fever (>38.5°C or 101.3°F)
• Chills, rigors
• Nausea, vomiting
• Flank pain
• Costovertebral angle tenderness (CVA tenderness)
• Dysuria and urinary urgency and frequency
• Cloudy and foul-smelling urine
• Pyuria (pus in urine), bacteriuria, and hematuria
• Sepsis (in severe cases) with hypotension, tachycardia, and altered mental status

Symptoms of Chronic Pyelonephritis

• Mild or asymptomatic in early stages
• Polyuria and nocturia (due to tubular damage)
• Hypertension (due to nephron loss)
• Proteinuria (glomerular involvement)
• Recurrent UTIs with vague symptoms

Pyelonephritis Treatment and Medical Management

• Includes hospitalization, hydration with IV fluids (Normal saline or Lactated Ringer's), with monitoring electrolytes
• Antibiotic therapy depends on severity, resistance patterns, and patient factors
  • Fluoroquinolones are first-line treatment for outpatient pyelonephritis
  • Cephalosporins are first-line for inpatient or severe cases - Carbapenems can be used for multi-drug resistant pyelonephritis - Aminoglycosides can be used for severe pyelonephritis
• Pain and fever can be managed with acetaminophen
  • NSAIDs should be AVOIDED

Antibiotic Therapy

• Fluoroquinolones for Outpatient Pyelonephritis
  • Examples include Ciprofloxacin and Levofloxacin
  • MOA: Inhibits bacterial DNA gyrase and topoisomerase IV, preventing bacterial DNA replication
  • Indications include uncomplicated acute pyelonephritis in stable patients
  • Contraindications include Pregnancy (category C) and Myasthenia gravis
  • Side Effects: Tendon rupture (Black Box Warning), QT prolongation (arrhythmias), and CNS effects

Cephalosporins for Inpatient/Severe Cases

• Examples include Ceftriaxone (3rd gen) and Cefepime (4th gen)
• MOA: inhibits bacterial cell wall synthesis, leading to cell lysis
• Indications: severe pyelonephritis requiring hospitalization, and pregnant patients
• Side effects include diarrhea and allergic reactions
• Risk of Pseudomembranous colitis (C. difficile infection)

Carbapenems for Multi-Drug Resistant Pyelonephritis

• Examples: Meropenem and Ertapenem
• MOA: inhibits peptidoglycan synthesis, causing bacterial death
• Indications include resistant organisms (ESBL-producing Enterobacteriaceae) and septic pyelonephritis
• Contraindications History of anaphylactic reaction to penicillins and may cause seizures at high doses

Aminoglycosides for Severe Pyelonephritis

• Examples: Gentamicin and Tobramycin
• MOA: Binds to 30S ribosomal subunit, inhibiting protein synthesis
• Indications include severe pyelonephritis with sepsis
• Contraindications include renal failure which is nephrotoxic and pregnancy which is ototoxic to fetus
• Side Effects: Nephrotoxicity, ototoxicity (aminoglycosides)

Urolithiasis

• Urolithiasis is when stones (calculi) from in the urinary tract
• This includes the kidneys(nephrolithiasis), ureters(ureterolithiasis), bladder(cystolithiasis), and urethra(urethrolithiasis)
• These stones develop due to supersaturation of urine with insoluble substances
• This leads to crystallization, aggregation, and stone formation

Epidemiology

• 8% persons in the United States
• More common in men
• Whites > Blacks

Risk Factors

• 50% of first-time stone formers develop another stone within 10 years
• There is a family history of urolithiasis
• Industrialized countries have higher rates
• Malabsorption conditions cause a higher rate (ex: Crohn's)

Types of Kidney Stones

Calcium Oxalate Stones (Most Common - 75-80%)

• Formed due to hypercalciuria, hyperoxaluria, hypocitraturia
  • Causes: Hyperparathyroidism (↑ Ca2+) and excessive dietary oxalate intake (spinach, rhubarb, nuts)
  • Malabsorption disorders (Crohn's disease, gastric bypass)

Calcium Phosphate Stones (10%)

• Are associated with alkaline urine
  • Causes: Renal tubular acidosis (RTA) type 1 and Hyperparathyroidism

Uric Acid Stones (5-10%)

• Associated with acidic urine (pH < 5.5)
• Main causes include: Gout (↑ uric acid), High purine diet (red meat, alcohol, shellfish), and Tumor lysis syndrome (chemotherapy)

Struvite (Magnesium Ammonium Phosphate) Stones (10-15%)

• Also called "Staghorn calculi"
• Associated with UTIs caused by urease-producing bacteria such as Proteus mirabilis, Klebsiella, and Ureaplasma urealyticum
  • pathogenesis: Bacteria produce urease → breaks down urea into ammonia (NH3).
  • Alkalinization of urine → precipitation of phosphate and magnesium

Cystine Stones (1-2%)

• Genetic disorder resulting in Cystinuria where there is defective transport of cystine in kidneys

Mechanism of Stone Formation

Supersaturation

• occurs when there is excess calcium, oxalate, phosphate, uric acid, or cystine in urine

Nucleation

• Formation of small crystal nuclei in renal tubules

Crystal Growth & Aggregation

• Occurs when Nuclei aggregate into larger stones

Retention in the Kidney

• occurs with stones lodge in the renal calyces, pelvis, or ureters, causing obstruction and pain

Clinical Manifestations

• Severe colicky pain (intermittent, flank-to-groin)
• Hematuria (Gross or Microscopic)
• Dysuria, urgency,and frequency are common
• Nausea, vomiting (due to autonomic response) is common
• Costovertebral angle (CVA) tenderness
• Urinary obstruction → Hydronephrosis (swelling of kidney due to urine retention)

Urolithiasis Medical Management

• Treatment: 50% pass spontaneously
• NSAIDs (First-Line): Examples: Ketorolac (Toradol), Ibuprofen, Naproxen
  • MOA: Inhibits COX-1 and COX-2, reducing prostaglandin synthesis → reduces inflammation and pain
  • Indications: Mild to moderate renal colic
  • Contraindications: CKD, GI ulcers, pregnancy
  • Side Effects: GI bleeding, nephrotoxicity
• Opioids (For Severe Pain): Examples: Morphine and Hydromorphone
  • MOA: Binds to μ-opioid receptors, providing analgesia
  • Indications: Severe renal colic (refractory to NSAIDs)
  • Contraindications: Respiratory depression, opioid dependency
  • Side Effects: Sedation, nausea, and constipation

Stone Expulsion Therapy (For Ureteral Stones <10mm)

Alpha-Blockers

• Examples: Tamsulosin and Doxazosin - MOA: Relaxes smooth muscle of the ureter, facilitating stone passage - Indications: Distal ureteral stones ≤10mm - Side Effects: Hypotension, dizziness, retrograde ejaculation

Calcium Channel Blockers

• Example: Nifedipine
  • MOA: Relaxes ureteral smooth muscle
  • Indications: Alternative to alpha-blockers

Stone-Specific Medical Management

For Calcium Stones

Thiazide Diuretics (Hydrochlorothiazide, Chlorthalidone)

 - MOA: Reduces calcium excretion in urine by increasing calcium reabsorption in the distal tubule
  - Indications: Recurrent calcium nephrolithiasis
  - Side Effects: Hypokalemia, hypercalcemia, hyperuricemia

Potassium Citrate

MOA: Alkalinizes urine, preventing calcium crystallization - Indications: Hypocitraturia-related calcium stones

For Uric Acid Stones

Allopurinol

  - MOA: Inhibits xanthine oxidase, reducing uric acid production
  - Indications: Hyperuricemia-related stones
 - Side Effects: Rash, hepatotoxicity, Stevens-Johnson Syndrome

Potassium Citrate

MOA: Alkalinizes urine, dissolving uric acid stones

For Struvite Stones

Antibiotics (For UTI), Examples: Ceftriaxone and Ciprofloxacin - MOA: Eliminates urease-producing bacteria Surgical Removal is necessary where struvite stones usually require percutaneous nephrolithotomy (PCNL)

For Cystine Stones

D-Penicillamine or Tiopronin - MOA: Binds to cystine, forming soluble complexes - Indications: Cystinuria-related stones

Hydration & Dietary Modifications

• Fluid intake exceeding >2.5L/day to prevent stone formation
• Following a low sodium diet
• Avoiding oxalate-rich foods like spinach, nuts, and tea
• Limiting animal protein

Acute Kidney Injury

Anatomy Review

• The main roles of the kidneys are to filter blood, remove waste, and maintain electrolyte and acid-base balance
• They regulate blood and pressure
• Activate Vitamin D
• Produce erythropoietin

Kidney Failure Effects

• Increase in waste in the circulation
• Disequilibrium of fluids and electrolytes
• Decreased activation of Vitamin D = decreased calcium absorption
• Decreased erythropoietin = anemia

Basic Definition

• Acute Kidney Injury (AKI), previously termed acute renal failure (ARF), represents a rapid decline in kidney function
• This is characterized by a rapid rise in serum creatinine and/or decrease in urine output over hours to days
• AKI disrupts fluid/electrolyte and acid-base and can lead to metabolic disturbances, volume overload, and uremia

Renal Failure Types

There are three categories of locations for renal failures

• PRERENAL FAILURE where the kidney fails because of decreased blood supply, or reduced renal profusion
• INTRINSIC/INTRARENAL FAILURE meaning the kidney failed because of a problem in the nephron
• POSTRENAL FAILURE which is renal failure in the collection system.

Pre Renal Failure

Kidneys are not receiving enough blood even though the organs are inherently functional and healthy - Hypotension - Shock - Hypovolemia or Hemorrhage - CAD within renal arteries

Effective Volume Depletion

• Kidneys will try to reabsorb sodium and water in an attempt to increase intravascular volume
• A large effective volume depletion includes;
  • CHF (Heart does not pump adequately which leads to decreased renal perfusion)
  • Cirrhosis: Scarring within the liver impedes blood flow in the hepatic portal system (portal hypertension)
  • Blood pools in the mesenteric system decreased blood reaching the kidneys (hepato-renal syndrome)

Intrinsic/Intra Renal Failure

• Caused by issue within the kidneys and kidneys no longer filter
  • Diseases of the glomeruli cause Nephrotic or Nephritic syndrome
  • Diseases of the tubule such as- Acute Tubular Necrosis, Drugs: , Ischemia

Post Renal Failure

• The Post renal failure category includes problems that impact the kidneys because the urine is being prohibited
  • Causes include;
    • Renal Stones
    • Tumor
    • Enlarged prostate
    • Edematous stomas

Treatment of Renal Failure

Fluid Resuscitation & Volume Management

• For Prerenal AKI from Hypovolemia:

  • Isotonic IV fluids (Normal saline, Lactated Ringer's)
  • Expands intravascular volume, increasing renal perfusion)

• Indications is Dehydration, hypotension, hemorrhage

• Contraindications is Heart failure and pulmonary edema

• Albumin (Colloid Fluid):

  • Indications: Hypoalbuminemia (severe burns, cirrhosis)

For Fluid Overload which can cause Oliguric AKI

• Loop Diuretics such as Furosemide works by Inhibiting the Na-K-2CI transporter in loop of Henle.
• This has an impact of diuresis causing side effects like hypokalemia, ototoxicity, dehydration

Electrolyte Management can require

Calcium Gluconate with hyperkalemia (K+ >5.5 mEq/L). This stabilizes the Cardiac Membrane

• Sodium Polystyrene Sulfonate (Kayexalate) exchanges exchanged Na+ for K+ in the gut
• Insulin + Dextrose: Shifts K+ intracellularly
• Loop Diuretics (Furosemide): Promotes renal K+ excretion

Acid-Base Balance is also critical so

Sodium Bicarbonate be also added to Neutralizes acid

Avoidance of Nephrotoxins

• Nephrotoxins are to be avoided or have dose adjusted in AKI
  • Aminoglycosides (Gentamicin, Tobramycin)
  • NSAIDs (Ibuprofen, Naproxen) reduces the beneficial renal perfusion
  • ACE Inhibitors (Lisinopril, Enalapril) should be cautiously prescribed in prerenal AKI

Chronic Kidney Disease (CKD)

Epidemiology: •One in seven Americans suffer from this affiction, or roughly 37 million •Higher incidence rates affect 60+

Increased Risk Factors

• Diabetes
• Hypertension
• Hyperlipidemia
• Smoking
• Recreational drug use
• NSAIDs
• Obesity

Pathophysiology

• Pathophysiology: End Stage Renal Disease (ERSD) where there is progressive, irreversible loss of kidney function

Increased Lab Values

• BUN, Creatinine, Sodium, Potassium, Hydrogen ions, Magnesium, Ammonia, Phosphate

Decreased Lab Values

• Calcium and Creatinine Clearance

Clinical and Medical Manifestations

Increased sodium and fluid Hypertension, Heart failure, or Pulmonary edema Sodium intake may need to be reduced and/or restricted Decreased potassium, and increased lethality in arrhythmias Impaired metabolic waste elimination is also common Impaired metabolic waste elimination (Nausea, vomiting, anorexia, and neurological symptoms.) The body lacks the materials needed, so is forces bone to break down.

Endocrine Complications and Medical Management

• Endocrine – increased parathyroid hormone (PTH) Chronic anemia, where erthropotien becomes reduced

Treatment for Kidney Disorders

Medical management—Treatment

• Renal replacement therapy
  • Support and maintenance of kidney for the life span, -Preventing futher complications

Renal replacement therapies (RRTs)

• artificial processes to remove the waste and liquids the body would use while the body is functional
• Intermittent hemodialysis (HD): hemodialysis
• peritoneal dialysis (PD).

Semi-permeable membrane usage is where process by which blood is separated from a dialysis solution is made possible

     -Artifical mambrane
    - Peritoneal membrane

Hemodialysis

Works across the blood stream, for about 3-4 tiems a wekk

• Diffusion: Solutes and water move across the membrane Movement across a concentration gradient, supported bythe addition of dialysate to the circuit
• Filtration:Movement of water driven by a hydrostatic pressure gradient
• Adsorption: Molecular adherence to the surface or interior of the membrane
• Convection: The forced movement of solutes with fluid(Solvent Drag)

####Water filtration Water and some smaller solutes can pass freely across semipermeable membranes -Passive transport: 1) movement of solutes from high concentration to lo concentration requiring no energy.

 -Water transport:
   - Active transport

Hemofilter processes

• Blood Device is used mainly support the execratory functions of the kidney Filers waste fromthe body

Key Process

• Hemodialysis, as it provides vascular access
• Peritoneal Dialysis Patient will likely have has high flexibility, with option to choose treatment

Peritoneal Dialysis

• It avoids rapid fluctuations in extracellular fluid composition The vascular membrane in peritonial cavity and the dialization -Solutes and reminants gets removed by diffusion -Fluid Process has 3 phases including the phase

Phase 1: First Fill

The sterile and temoerature dialisate is set up from tubing

Phase 2: Dwell Phase

Body fluid remains in body -waste and electrolytes diffuse from the the diaslite the the remainders -water is controlled using dextrose in the dialysis

Phase 3 : Drain Phase

Gravity is then used to drain the fluid after the period

Clinical Differences in PD,

Continuous Ambulatory, Dialysis is a treatment for four or 5 at 4-6 hours with the daily time is usually used without the patients needs are over night

Automated peritonial treatment is also comon, and uses cycler and is a multiple over night method to achieve 30 mi cycle during phase

NON- Eligible patients would consist of the following

• Colostomy -Disc Damage

Syphilis

Primary Infection

• Occurs 10-90 days post infection Chancre at site of inoculation that begins as papule then ulcerates with a hard edge and clean, yellow base
• -Indurated and painless
• -Usually located on genitalia
• -May be solitary or multiple
• -Persists 1-5 weeks then health spontaneously
• -Regional lymphadenopathy

Secondary syphilis

• 17 days to 6 months post infection
• rash Bilaterally symmetrical, polymorphic, nonpruritic, frequently on soles and palms
• It Persists for 2-3 weeks before resolving spontaneously
• Key feature
• condyloma lata: moist, pink, peripheral warty lesions, may be present on glans, perianal, and vulval areas, and intertriginous areas
• Mucous patches in mouth, throat, and cervix
• Flu-like symptoms
• --Mild hepatosplenomegaly
• --Generalized lymphadenopathy

Latent syphilis

• --Asymptomatic
• --2 to 30 plus years post infection

Tertiary syphilis

---2 to 30 plus years post infection

• Cardiovascular manifestations: aortic valve disease, aneurysms
• Neurologic manifestations: are the biggest concern of this stage including meningitis, encephalitis, dementia
• Integumentary manifestations: gumma
• Orthopedic manifestations: Charcot joints, osteomyelitis

Treatment of Syphillus

Medical management—Diagnosis include series of clinical and lab test

• ---Serological testing uses a nontreponemal test and a treponemal test.
• -----Nontreponemal tests (presumptive tests) include rapid plasma regain (RPR)
• -----Treponemal tests (positive for life after treatment) use Fluorescent treponemal antibody absorbed (FTA-ABS)
• -----Microscopy for testing and diagnosis is common place also
• --Medical management of treatment can also be done with usage of various medications like:
• ----Penicillin, Doxycycile and Tertracycline

Genital Herpes

Epidemiology shows it is common spread,

• -HSV-1 prevalence 47.8% in US
• -HSV-2 prevalence 11.9% aged 14 to 49 Pathophysiology includes:
• --Highly contagious through skin, a lot of patients are infected and unaware
• ---Transmission to others may occur unknowingly

Symptoms and Side Effects

Includes episodeatic outbreakes with clear cesciles

Types of infection

• Medical management 1One or more clear vesicles
• ----- Vescile rupture and forming of painful ulcers is also common

Infection

• Visual inspection
• Cell culture
• Polymerase chain reaction testing Medical management —Treatment Anti-vural and anti- infectations 1.Acyclovir 400mg TID for 7-10 days 2.Famciclovir 250mg TID for 7-10 days Valacyclovir 1g BID for 7-10 day Chlamydia Trachomatis is a STI Most common with 129 Million cases

####Pathophysiology

• --C. Trachromatis transmission and and incubation in 21 day, Often presents without systoms for males and females, and will like present with Edema, Vagina, or Cervical Tenderness(Dysuria/Puoria

Other SymptomsInclude

• --Pelvic Pain and inflimation
• --Proctitis infmalation and swelling
• --Burnig and infalimation

####Medical management

• -Diagnose with swaps Treat with Doxycyline

####### Diagnosis NAAT is Most Specific or Selective Medical management:

• -Medicate with Doxcycline

Medical management of Gonherria and Chlymidia

1.Rocephin is the the PREFERRED drug for first like treatment by a a mile -if the patient is over 50 kilo, the dosage will need to be increased A mix of ceixime and azithromycin and doxyciline can also be precribes, but less effective Gentamecin can bee effective, as long as the the other allergies do not pose to much of risk.